This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. We are continuing to investigate the role of 53BP1 in protecting DNA ends during repair, continuing the work published recently in Cell (53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks Bunting SF, Call[unreadable]n E, Wong N, Chen HT, Polato F, Gunn A, Bothmer A, Feldhahn N, Fernandez-Capetillo O, Cao L, Xu X, Deng CX, Finkel T, Nussenzweig M, Stark JM, Nussenzweig A. Cell. 2010 41(2):243-54) This protein is required for end protection during repair but we think that the effect is indirect and due to some associated protein or proteins. We have developed cell lines expressing tagged forms of the protein and phospho-mutants that are deficient in the end protection activity and a method for tandem purification based on two tags.